Hippocampus/Memory Flashcards

1
Q

explicit memory

A

“that”

  • true/false
  • involves modeling of external world
  • storage of facts/episodes
  • highly flexible; many components
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2
Q

implicit memroy

A

“how”

  • not propositional (procedural)
  • change in skilled behavior
  • not conscious- motor learning
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3
Q

explicit memory is broken down into

A

episodic–memory of personal experience

semantic– words/concepts

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4
Q

structures involved in formation of explicit memory

A

hippocampus proper
dentate gyrus
subiculum
entorhinal cortex

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5
Q

R hippocampus

A

spatial information

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6
Q

L hippocampus

A

objects

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7
Q

4 phases of explicit memory

A

1) encoding– new info is attended to and linked to existing information
2) storage- mechanism/actual brain parts of memory retention
3) consolidation- temporary to permanent
4) retrieval- recall

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8
Q

medial temporal lobe

A

foramtion of new memories, but stored elsewhere

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9
Q

short term/working memory

A

PFC
two components
- verbal information
-visuospatial information

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10
Q

efficacy can be changed by

A

modulating neurons in PFC

  • ACH on muscarinic receptors–>change Ca2+ act on nonselective cation channels
  • act D1 dopamine R: working memory best when in intermediate range
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11
Q

long term potentiation involves

A
functional changes in
-# post syn R
- post syn R channel fx
- presyn NT release
structural changes in
- # post syn spines (new synapses vs elim)
- size os spine heads
- spine stability
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12
Q

perfornat pathway

A

axons from entor cells–>granule cells ind entate gyrus–>pyramidal cells CA3 of hippocampus (mossy fiber pathway) GLUTAMATE–>pyramidal neurons of CA1 (schaffer collaterals)–>back to entorinal/subiculum

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13
Q

neurophysiolo postulate

A

following a high level of presyn activation, the size of synaptic field potentials (epsp amplitudes) in CA1 post syn neurons are larger than they were before and response remains long after presyn activity decreases

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14
Q

damage to place cells

A

cannot do water maze

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15
Q

LTP characterized by

A
  • induction (bchemical process that arise from high levels of activation)
  • expression (long term structural and functional changes)
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16
Q

to induce LTP

A

presyn high lvel activity
post syn must depol
act on AMPA and NMDA
influx Ca into cell

17
Q

at rest

A

low levels of glutamate bind AMPA R–>small depolarization

glutamate binds NMDA R–> no current because Mg2+ binds channel

18
Q

high levels presyn activity

A

more glutamate–>act AMPA R–>large depol (-40mv)–>Mg2+ repelled from NMDA R–>positive ion flow into cell–greater depolarization

19
Q

NMDA therefore acts as a

A

coincidence detector

pharm blockers or deletion (cre/lox) inhibit LTP

20
Q

Ca into cell

A

activates a set of kinases (PKA, PKC, CAMKII)
1) inserts new AMPA R from vesicles at spine head
2) phos AMPAR (stabilizes, greater ion flux increases sensitivity)
3) dynamic restructing of actin cytoskeletion (enlargement, new spines)
4) increasd release of glut from presyn cel
(NO synthase–phos by CAMKII–>makes NO–>locally diffuse to presyn terminal

21
Q

BDNF

A

places a role in postsyn ampa r insertion

22
Q

ltp does/does not req gene expression

A

DOES

CAMKII, PKA, PKC act downstream to change gene transcription

23
Q

epigenetics

A

kinase phos KREB–>interacts with CBP –>histone acetylation–>restructures chromatin

24
Q

fear

A

enhanced meth of BDNF gene–>inhibits BDNF expression–>impairs hippocamp role in contextual fear memory

25
Q

purpse of LTD

A

erase imporatance of previously held memories in stressful situations so can focus on whats at hand

26
Q

stress

A
hippocampal neurons-->express both classical and gCC R and membrane gCC R-->changes kinase signaling
increases glut (therefore increases AMPA R)
increase LTD, dec LTP
->paradoxical, but resest threshold of lTP when something new need to be learned?